Gladstone Institute of Virology and Immunology, University of California, San Francisco, CA 94158, USA.
Mol Aspects Med. 2010 Oct;31(5):383-97. doi: 10.1016/j.mam.2010.06.001. Epub 2010 Jun 9.
The Vif protein of HIV is essential for the effective propagation of this pathogenic retrovirus in vivo. Vif acts by preventing virion encapsidation of two potent antiviral factors, the APOBEC3G and APOBEC3F cytidine deaminases. Decreased encapsidation in part involves Vif-mediated recruitment of a ubiquitin E3 ligase complex that promotes polyubiquitylation and proteasome-mediated degradation of APOBEC3G/F. The resultant decline in intracellular levels of these enzymes leads to decreased encapsidation of APOBECG/F into budding virions. This review discusses recent advances in our understanding of the dynamic interplay of Vif with the antiviral APOBEC3 enzymes.
HIV 的 Vif 蛋白对于该致病性逆转录病毒在体内的有效繁殖是必不可少的。Vif 通过防止两种有效的抗病毒因子,即 APOBEC3G 和 APOBEC3F 胞苷脱氨酶的病毒衣壳包裹来发挥作用。部分衣壳包裹减少涉及 Vif 介导的募集一种泛素 E3 连接酶复合物,该复合物促进 APOBEC3G/F 的多泛素化和蛋白酶体介导的降解。这些酶在细胞内水平的下降导致 APOBECG/F 较少包裹到出芽的病毒粒子中。这篇综述讨论了我们对 Vif 与抗病毒 APOBEC3 酶之间动态相互作用的理解的最新进展。